Abstract
Celiac disease (CD) is an immune mediated disorder characterized by intolerance to glutens in certain grains like wheat, barley, and rye. The gliadin exposure in susceptible individuals leads to an inflammatory reaction with damage to the small intestinal mucosa with villous blunting, atrophy and ultimate disappearance of intestinal villi. The damaged intestinal villi lead to malabsorption.
The development of celiac disease (CD) is determined by both environmental and genetic factors. The gluten in the grains represents an environmental factor. In addition to this environmental factor, CD development involves genetic predisposition as most CD patients possess human leucocyte antigen (HLA) DQ2 and/or HLA-DQ8. The complex interplay of multiple genetic and environmental factors determines the development of CD.
Small bowel mucosal biopsies remain gold standard for the diagnosis of CD because of variation in the clinical findings and serologic testing. Histologic examination of small intestine also helps to monitor the course of disease, response to treatment, and in detecting potential complications of celiac disease such as enteropathy associated T-cell lymphoma, adenocarcinoma, and concurrent intestinal diseases.
There has been significant development in understanding the pathophysiology, pathogenesis, and diagnosis of celiac disease. The present review summarizes the important development in CD in last few years with special emphasis on etiopathogenesis, pathophysiology, and pathologic features of CD. Better understanding of these features is not only important for correct diagnosis but also results in better patient management and would pave a way for future research of this overly complex disease characterized by complex interaction of environmental, genetic as well as immunologic mechanisms.